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Steroids and Diabetes June James Steroids and Diabetes June James

Steroids and Diabetes June James - PowerPoint Presentation

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Steroids and Diabetes June James - PPT Presentation

Associate Professor University of Leicester Nurse Consultant University Hospitals of Leicester NHS Trust July 2017 Leaning objectives At the end of this session you should be able to Discuss the implications of steroid ID: 1014306

insulin diabetes steroid glucose diabetes insulin glucose steroid blood hyperglycaemia dose pre treatment steroids mmol people care existing mgs

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2. Steroids and DiabetesJune JamesAssociate Professor- University of Leicester Nurse Consultant- University Hospitals of Leicester NHS Trust July 2017

3. Leaning objectivesAt the end of this session you should be able to:Discuss the implications of steroid use and diabetes Review treatments for steroid induced hyperglycaemiaIdentify use in different groups including:People with known diabetes People not known to have diabetesPregnancy End of life care

4. Case study 62 years man. Weight 102kg, BMI 32 kg/m2T2DM on Metformin.HbA1c 55 mmol/mol Background:COPD, CVA, IHD Respiratory clinic’….progressive dyspnoea Plan:Prednisolone 30 mg for 10 days then reduced to 20 mg for one week and then to reduce to 10 mg maintenance for now.Follow-up: 2/12

5. 3 weeks laterAcute admissionOsmotic symptoms, BG 32 mmol/LHba1c 112 mmol/mol48 hrs in patient stay over weekendGliclazide (SU) , followed by insulin6 months OPD in diabetes clinic discharged OHA, HbA1c 44mmol/mol

6. Background0.75% use steroids40% for respiratory problemsInpatient use >10%Most use for <5 days, but 22% is for > 6 months and 4.3% for > 5 yearshttps://www.nos.org.uk/NetCommunity/Document.Doc?id=422Fardet L et al Rheumatology 2011;50(11):1982-1990

7. Background There are no reliable estimates for prevalence of glucocorticoid use in hospital/ community We don’t know if more people in hospital are on steroids, and if so are the doses used usually higher than those used in community?The prevalence of undiagnosed diabetes in hospitalised patients may be ~18% Wexler DJ et al JCEM 2008;93(11):4238-4244

8. Steroid regimens Once a day –short course (Prednisolone 30 mg OD for 5 days) Multiple dose (Dexamethasone BD/TDS) High dose short duration (methyl prednisolone 3 days/ 5 days) High dose infrequent (Oncology) Betamethasone x 2 doses ( Pregnancy )

9. People at risk of hyperglycaemia Pre-existing type 1 or type 2 diabetesPeople at increased risk of diabetes. Impaired glucose regulation - HbA1c 42-47mmol/molPeople previously hyperglycaemic with steroid therapy

10. Commonly used steroids

11. Normal physiologyThe adrenal glands produce cortisol that is equivalent to about 7.5mg of prednisolone dailyAny doses higher than this will lead to problems with carbohydrate metabolism

12. Doses > 7.5mg of prednisolone for more than 2 weeks than this causes adrenal suppression Too rapid a withdrawal will lead to hypo –adrenalism demonstrated by:recurrent hypoglycaemia,hypotensionhyponatraemia, hyperkalaemia

13. How do “steroids” work?Acutely increases hepatic glucose production Complex effects on β-cell function and may reduce insulin production They promote visceral adipose tissue deposition and enhance lipolysisAlter levels of adipose tissue derived hormones and cytokinesSaltiel AR et al Nature 2001;414:799-806 Hollingdal M et al Diabetologia 2002;45:49-55Boyle PJ Diabetes Reviews 1993;1:301Lambillotte C et al J Clin Invest 1997;99:414-423Petersons CJ et al Diabetes Care 2013;36:2822-2829

14. Glucose inhibitionStarts very early after steroid ingestionIn (previously well controlled) patients leads to postprandial hyperglycaemiaHyperglycaemia may be a transient rise of blood glucose levels or may result in HHSThe best predictors of glucocorticoid-induced diabetes are family history of diabetes, increasing age, and glucocorticoid dose Schacke H et al Pharmacol Ther 2002;96:23-43Dimitriadis G et al Biochem J 1997;321:707–712Petersons CJ et al Diabetes Care 2013;36:2822-2829

15. Now we know the cause, what’s the treatment?Education and pre-empting the (almost) inevitableLetting teams know that when someone starts corticosteroid treatment that blood glucose levels are very likely to rise and to watch for itWhen it happens, treat early

16. What is the best treatment? GlitazonesDPP-4sSGLT2 Inhibitors GLP- 1RAs SulphonylureasInsulin

17. Gltizones…..Work very slowly – so may have been useful in an outpatient settingSeveral controversies abound regarding the use of glitazones, so their use is decliningIncreased CV death ratesIncreased fracture ratesIncreased rates of macular oedemaNissen SE NEJM 2007;356(24):2457-2471Loke YK et al CMAJ 2009;180(1):32-39Ryan EH et al Retina 2006; 26(5):562-70Ferwana M et al Diabetic Med 2013;30(9):1026-1032

18. GLP-1’s/ DDP-4sSGLT2is - Little experience with steroid use - Do not have a fast response to reducing hyperglycaemia GLP1s - reduce blood glucose but: - Little experience/ evidence with steroid use -It makes people who are already unwell feel nauseated -Not appropriate for people who are NBM -Do not have a fast response to reducing hyperglycaemia DPP-IV antagonists - limited published data on the use with steroids, e.g. Umpierrez using Sitagliptin in 90 hospitalised patientsUmpierrez GE et al Diabetes Care 2013

19. Sulphonylureas SU - GliclazideTitrate from 40 mgs am to 240 mg amYou may want to contact the specialist team if you are concerned re high Gliclazide doses Also add in up to 80 mgs pm ( max 320 mgs per day )Insulin often requiredVarious regimensVRII

20. InsulinInsulin is recommended as the drug of choice for the treatment of glucocorticoid-induced hyperglycaemiaPrandial insulin should minimise the effects of the postprandial rise in glucose For patients receiving high-dose intravenous glucocorticoids, an intravenous insulin infusion may be appropriate Hirsch IB et al Endocr Metab Clin North Am 1997;26:631–645

21. However!How much insulin should be given in the insulin naïveWhat about dose increases in people already on insulinShould you give it IV or SC

22. IV Insulin Intravenous infusions tend to achieve acceptable blood glucose concentrations quicker than MDIAn insulin infusion allows appropriate tapering of insulin infusion ratesGlycaemic control is not compromisedHypoglycaemic risks can be minimised – especially with high dose steroids

23. What About Subcutaneous Insulin? IV insulin is not the answer for all – but maybe if the blood glucose is consistently above ~15 mmol/LMay need a basal bolus regimenNo work has been done to compare human with analogue insulin in this field

24. Should “steroid induced” hyperglycaemia always be treated (pre-existing diabetes)No clinical studies/ evidence to tell us However - hyperglycaemia in a hospital setting (for any cause) is associated with poor mortality, morbidity, and health economic outcomes Improving glycaemic control improves these outcomesUmpierrez GE et al J Clin Endocrinol Metab 2002; 87:978–982Bruno A et al Diabetes Care 2008;31(11):2209-2210

25. Which insulin? Intermediate acting human basal insulinOnce a dayGradually up titrationAnalogue basal insulin if:– if hyperglycaemia throughout day– early morning hypos!

26. Factors to consider during treatment Risk of hyperglycaemia and hypoglycaemia Duration of steroid therapy Pre-existing diabetesCo-morbidities

27. JBDS targets (UK)Inpatient blood glucose readings of 6 -10 mmol/l recommended but 4 -12 mmol/l is acceptableAvoid wide swings in CBG

28. Pre existing diabetesType 2On non insulin therapiesTitrate oral medications Add Gliclazide and titrate to 240 mgs am/ 80 mgs pm Type 1 and 2 Insulin treated patients- Increase morning dose of premixed insulin- Increase bolus at lunch/teaShift basal to morning Test four times a dayIf capillary >12mmol/L on two occasions during 24 hours, then review treatment

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30. Steroid induced diabetesOnce a day BG monitoringPre lunch or evening mealIf BG >12 increase frequency to 4/dayIf 2 or more BG >12 mmol/l -TREAT

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32. PregnancyBetamethasone - lung maturityHyperglycaemia 24 -72 hrsRisk - GDM Pre-existing diabetes -VRIIUp to 40% increment in dose

33. End of life Consider stages of end of lifeHyperglycaemia may be complicated by use of food supplements Keep BG 6-15 mmols No fasting BG readings No HbA1c targets

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35. Steroids commenced in hospital and patient discharged (No known diabetes) Standard education for the individual and carer Blood glucose testing once daily (pre or post lunch or evening meal) If blood glucose readings greater than 12mmol/L increase frequency of testing to four times daily If two consecutive blood glucose readings greater than 12mmol/L in a 24 hour period follow algorithm for management of steroid induced diabetesIf hyperglycaemia resolved stop CBG testing and arrange definitive test for diabetes

36. Hospital discharge (Known diabetes) Standard education for patient and carer including advice on hypoglycaemia Continue CBG monitoring until blood glucose normalises (4 -7mmol/L)Review by agreed individual (e.g. GP, Diabetologist, DSN/ PN) at an appropriate juncture to consider down-titration of antihyperglycaemic therapy if necessary

37. Education Steroids are often started by health care professional who may not have experience of managing diabetesPatients with or without pre-existing diabetes will need to be aware of the impact steroid therapy makes on glycaemia control. Monitoring and treatment

38. Summary Steroid use will result in hyperglycaemia in most casesTreatment algorithms are available There is consensus guidelines but no real evidence of appropriate treatment pathwaysThose with no previous diagnosis of diabetes will need to undergo screeningPatient and staff education should be put in place in localities

39. Resources